During aging, "lipofuscin" and "ceroid"-like pigments accummulate in nerve, liver and other cell types. These pigments were identified as peroxidized unsaturated lipids. Peroxidation of unsaturated fatty acids of phospholipids changes membrane fluidity, which, in turn, interferes with various parameters of drug-receptor interactions in the nervous system and oxidation of drugs by membrane and bond enzymes. Recent investigations indicate that two phospholipid-N-methyltransferases which convert phosphatidyl-ethanolamine to phosphatidylcholine regulate membrane fluidity, which brings about changes in drug-receptor interactions, and incorporation of drug-induced cytochrome P450 into liver microsomal membranes. Therefore, the primary objectives of this investigation are: (1) Concomitant variations in parameters of drug-receptor interactions in the cholineregic nervous system, membrane fluidity and membrane phospholipid-N-methyl-transferases as a function of age in experimental animals, and in ceroid-lipofuscin syndrome experimentally produced in tissues, cells and membranes by peroxidation; (2) Concomitant variations in membrane phospholipid-N-methyltransferases and cytochrome P450 levels in liver microsomes of experimental animals as a function of age, and in regenerated liver cells in aged rats; (3) Evaluation of drugs (e.g., Centrophenoxine) in aged rats and in experimental ceroid-lipofuscin syndrome for depletion of age pigments or protection against peroxidation. These investigations provided now relationships between aging membrane lipid peroxidation, cholinergic chemical transmission, and membrane fluidity.